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M S Gordeeva

Publications and source records attributed to M S Gordeeva.

9 recordsLinked to original sources
PubMed1989

[Delayed type hypersensitivity reaction in the pathogenesis and formation of immunity in tularemia infections in mice].

As a result of our studies, strain differences in the sensitivity of CBA and BALB/c mice to partially attenuated Francisella tularensis strain have been revealed. Relationship between the increased migration of lymphocytes to the liver and lymphoid organs and the intensive development of cell-mediated immunity reactions has been shown. An important role of local reactions (the skin at the site of the inoculation of F. tularessis + a regional lymph node) in the development of the pathological process and the formation of immunity to tularemia infection has been noted. A high level of resistance to F. tularensis strain used for inoculation in BALB/c mice seems to be greatly due to the fact that in these mice more intensive cell-mediated immunity reactions develop at the early stages of infection, than in CBA mice.

Animals↗
PubMed1985

[Lymphocyte migration in syngeneic lymph node implants].

Lymph nodes implanted subcutaneously to syngeneic recipients were shown to regenerate after mass cell destruction. Regenerated lymphoid tissue has a resemblance to the cortical zone of intact lymph nodes. Microenvironment of regenerated lymphoid tissue provides homing of lymphocytes. However, migration of 51Cr-labelled lymphocytes to implants declined drastically, as compared to lymphocyte migration to intact lymph nodes. Attenuation of proliferative activity and the data of morphological analysis indicate a more prolonged retention of lymphocytes in implanted lymph nodes. The results obtained could be attributable to only partial recovery of sinus and vessel systems regulating the inflow and outflow of lymphocytes in lymph nodes.

Animals↗
PubMed1975

[The effect of polysaccharide from typhoid bacteria on hemopoietic stem cells].

A study was made of dynamics of the content of colony-forming units (CFU) in the spleen and the bone marrow of the nonirradiated F1 (CBA times C57BL) mice to which polysaccharide (PS) from typhoid bacilli was administered. A method of exogenous colony formation was used in this work. A single PS administration increased the CFU count in the bone marrow (2-2 1/2 times) and in the spleen (3 times). Repeated (6- and 9- time) administration of PS was not more effective than a single one. Apparently PS acted as an inductor which caused proliferation of the stem hemopoietic cells and maintained this process for a definite period of time automatically.

Animals↗
PubMedDate not supplied

[Effect of maternal virus-specific T-lymphocytes on pregnancy and fetal pathogenesis in experimental congenital influenza infection].

Inoculation of virus-specific cytotoxic lymphocytes (CTL) to pregnant mice infected with influenza virus was shown to result in a decrease of infectious virus concentration in the lungs and blood of mice as well as in the placentas and fetuses. With an increase in the dose of inoculated CTL, however, premature deliveries with stillbirths were observed as well as deaths of the mice, the highest frequency of fetal deaths being observed after infection of pregnant mice in the first half of pregnancy. It is not excluded that maternal virus-specific CTL played a role in the formation of developmental abnormalities and immunodeficient states in newborns.

Animals↗
PubMedDate not supplied

[The role of maternal virus-specific cytotoxic T-lymphocytes in the immunopathology of congenital influenza infection in mice].

Using 51Cr isotope label it was demonstrated that a very low per cent of syngeneic lymphocytes derived from healthy donors and inoculated in the blood stream of uninfected or influenza virus-infected pregnant mice is found in fetuses before delivery. Similar results were obtained after inoculation of virus-specific cytotoxic lymphocytes (CTL) into uninfected pregnant mice. After inoculation into the blood stream of infected pregnant mice of virus-specific CTL their migration into fetuses before delivery increases, being most marked in 25-30% of mice. Intravenous inoculation of excess CTL (10(6) cells) to infected pregnant mice resulted in rapid development of signs of slow influenza infection in the progeny with typical clinical picture and histopathological lesions in organs and tissues. Large doses (10(7)-10(8) cells) of CTL inoculated into the blood stream cause higher reduction and death of fetuses and increase the rate of stillbirths. The role of maternal virus-specific CTL in the pathogenesis of experimental congenital and especially slow influenza infection is discussed.

Animals↗